Metabolism of Vitamin A in White Adipose Tissue and Obesity

Jeyakumar, Shanmugam M.; Yasmeen, Rumana; Reichert, Barbara; Ziouzenkova, Ouliana

doi:10.1201/b14569-4

Cited by 10 publications

(15 citation statements)

References 170 publications

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“…Adipose tissues comprise two predominant types: white adipose tissue (WAT), and brown adipose tissue (BAT) [6, 10]. Although both types of adipose tissue influence obesity, they have opposite functions in energy balance regulation.…”

Section: Adipose Tissue Depotsmentioning

confidence: 99%

“…There are different types and locations of WAT depots, each having its unique heritable gene expression pattern [5, 17]. Each fat depot exerts systemic effects on energy homeostasis and inflammation [10]. WAT depots are named based on their location.…”

Section: Adipose Tissue Depotsmentioning

confidence: 99%

“…WAT stores a considerable amount of ROL and RE in lipid droplets, although vitamin A can be delivered to adipose tissue as retinol (ROL) and retinyl esters (RE) and RA in the circulation (reviewed in [10]). WAT is the second largest storage site of vitamin A after the liver.…”

Section: Intra/paracrine Effects Of Retinoic Acid Production From Vitmentioning

confidence: 99%

“…WAT is the second largest storage site of vitamin A after the liver. ROL is the major form of RA precursors carried in the blood bound to the retinol-binding protein (RBP4)-transthyretin (TTR) complex (reviewed in [10, 118]). ROL uptake from the RBP4 complex is mediated by STRA6 receptor in WAT [119, 120].…”

Section: Intra/paracrine Effects Of Retinoic Acid Production From Vitmentioning

confidence: 99%

“…The reverse conversion of ROL to RE is catalyzed by lecithin retinol acyltransferase (LRAT) [118]. In cytosol, ROL can be reversibly converted to Rald by short-chain reductases/dehydrogenases (SDR)/retinol dehydrogenase (RDH), the alcohol dehydrogenase (ADH), and aldo-ketoreductases families of enzymes (reviewed in [10]). Rald can be reduced to ROL by ADH and RDH families of enzymes or irreversibly oxidized to RA by the aldehyde dehydrogenase 1 (ALDH1) enzyme family (ALDH1A1, ALDH1A2, ALDH1A3) [reviewed in [132, 145]].…”

Section: Intra/paracrine Effects Of Retinoic Acid Production From Vitmentioning

confidence: 99%

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Enzymatic intracrine regulation of white adipose tissue

DiSilvestro

Petrosino

Aldoori

et al. 2014

Hormone Molecular Biology and Clinical Investigation

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Abdominal fat formation has become a permanent risk factor for metabolic syndrome and various cancers in one-third of the world's population of obese and even lean patients. Formation of abdominal fat involves additional mechanisms beyond an imbalance in energy intake and expenditure, which explains systemic obesity. In this review, we briefly summarized autonomous regulatory circuits that locally produce hormones from inactive precursors or nutrients for intra-/auto-/paracrine signaling in white adipose depots. Enzymatic pathways activating steroid and thyroid hormones in adipose depots were compared with enzymatic production of retinoic acid from vitamin A. We discussed the role of intracrine circuits in fat-depot functions and strategies to reduce abdominal adiposity through thermogenic adipocytes with interrupted generation of retinoic acid.

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Section: Adipose Tissue Depotsmentioning

confidence: 99%

Section: Adipose Tissue Depotsmentioning

confidence: 99%

Section: Intra/paracrine Effects Of Retinoic Acid Production From Vitmentioning

confidence: 99%

Section: Intra/paracrine Effects Of Retinoic Acid Production From Vitmentioning

confidence: 99%

Section: Intra/paracrine Effects Of Retinoic Acid Production From Vitmentioning

confidence: 99%

See 3 more Smart Citations

Enzymatic intracrine regulation of white adipose tissue

DiSilvestro

Petrosino

Aldoori

et al. 2014

Hormone Molecular Biology and Clinical Investigation

Self Cite

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Vitamin A and its metabolic pathway play a determinant role in high‐fructose‐induced triglyceride accumulation of the visceral adipose depot of male Wistar rats

Reddy

Mahesh

Munikumar

et al. 2019

Cell Biochemistry & Function

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Here, we tested a hypothesis that vitamin A and/or its metabolic pathways are involved in the high-fructose-mediated alteration in adipose tissue biology. For this purpose, weanling male Wistar rats were provided with one of the following diets: control (C), control with vitamin A deficiency (C-VAD), high fructose (HFr), and HFr with VAD (HFr-VAD) for 16 weeks, except that half of the C-VAD diet-fed rats were shifted to HFr diet (C-VAD(s)HFr), after 8-week period. Compared with control, feeding of HFr diet significantly increased the triglyceride content (P ≤ .01) and thus adipocyte size (hypertrophy) (P ≤ .001) in visceral adipose depot; retroperitoneal white adipose tissue (RPWAT) and these changes were corroborated with de novo lipogenesis, as evidenced by the increased glycerol-3-phosphate dehydrogenase activity (P ≤ .01) and up-regulation of lipogenic pathway transcripts, fructose transporter, and aldehyde dehydrogenase 1 A1. On the contrary, the absence of vitamin A in the HFr diet (HFr-VAD) failed to exert these changes; however, it induced adipocyte hyperplasia. Further, vitamin A deficiency-mediated changes were reversed by replenishment, as evident from the group that was shifted from C-VAD to HFr diet.In conclusion, vitamin A and its metabolic pathway play a key determinant role in the high-fructose-induced triglyceride accumulation and adipocyte hypertrophy of visceral white adipose depot.Significance of the study: Here, we report the metabolic impact of high-fructose feeding under vitamin A-sufficient and vitamin A-deficient conditions. Feeding of high-fructose diet induced triglyceride accumulation and adipocyte hypertrophy of the visceral white adipose depots. These changes corroborated with augmented expression of vitamin A and lipid metabolic pathway genes. Contrarily, absence of vitamin A in the high-fructose diet did not elicit such responses, while vitamin A

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